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Complications ofRevascularization 173
the bypass [27, 28], although it is important to make sure that there is no sig-
nificant disease in the inflow vessels. In some circumstances, a hybrid approach
of using endovascular options to treat the inflow and then a surgical bypass as
outflow are most appropriate [29]. An example of this would be a stent placed
in the SFA above a bypass from the above‐knee popliteal artery to the dorsalis
pedis artery in a patient with a foot ulcer and minimal autogenous vein to use
a conduit.
As in bypasses above the knee, vein is the preferred conduit, and its effect on
patency for targets below the knee is even more pronounced. Primary patency
rates for bypasses with prosthetic to the tibial arteries are as low as 30–39% at
3 years [30, 31]. Despite low primary patency rates, limb salvage can still be
accomplished in a proportion of patients if the tissue loss can heal prior to the
bypass occluding. In fact, the same studies reporting primary patency of
30–39% also reported limb salvage of 61–71% at 1 year in the same patients
[30, 31]. Depending on the specific anatomy of the patient, the patency rates
with a prosthetic bypass may be low enough to render the operation futile; this
is a decision best made by a specialist. In general, diffuse disease in the tibial
arteries predicts poor patency rates.
Below the knee, several technical considerations have been attempted to
improve the overall poor patency with prosthetic. A cuff of vein can be sewn
between the distal end of the prosthetic and the distal target vessel. There are
various configurations of vein cuffs, a detailed discussion of which is beyond
the scope of this chapter. Multiple small studies have been performed on the
use of these, and meta‐analyses have shown that they improve primary patency
[32] as well as limb salvage [33], although large randomized controlled trials
have not been performed. The intentional creation of arteriovenous fistulas to
improve outflow can also augment limb salvage rates [34].
In some patients with CLI, diffuse tibial disease gives way to patent vessels
within the foot. In selected circumstances, bypasses can be performed from
the below‐knee popliteal artery or tibial arteries themselves to patent vessels in
the foot. These cases can only be performed if there is adequate vein, as pros-
thetic grafts do not have acceptable patency rates. Series from select centers
report primary patency as high as 58–80% at 1 year, with an accompanying
limb salvage rate of 77–90% [35, 36].
Complications of Revascularization
Complications of revascularization include both systemic and local complica-
tions. Patients with vascular disease typically have multiple comorbidities, and
therefore complications must not be taken lightly.
Cardiac complications are a major cause of morbidity and mortality in
patients undergoing open revascularization given their overwhelming burden
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8 Surgical Management ofPeripheral Artery Disease
174
of atherosclerotic disease. Myocardial infarction occurs in 2.3–14% of patients
undergoing peripheral vascular procedures [37, 38]. Routine screening for
cardiac disease as well as preoperative cardiac optimization is recommended.
Peri‐operative beta‐blockade should be continued postoperatively in patients
who have an indication for it, but evidence is equivocal as to whether beta‐
blockade should be started on all vascular patients prior to undergoing vascu-
lar surgery [39, 40].
Respiratory complications following vascular procedures are more common
in patients undergoing thoracic procedures or who have a history of smoking.
Complications include atelectasis and pneumonia. Prevention, including pre-
operative optimization and aggressive pulmonary toilet postoperatively, is
crucial. The importance of smoking cessation cannot be overemphasized.
Renal failure can also occur following a vascular procedure. This is most often
due to acute tubular necrosis, either from ischemic injury in the case of an aor-
tic clamp above the renal arteries, atheroemboli, or toxic injury from contrast
dye. Acute tubular necrosis due to contrast dye can be prevented with hydration
pre‐ and postoperatively, with either normal saline or a sodium bicarbonate
infusion. An elevated creatinine preoperatively increases the risk of kidney
injury, but pre‐existing chronic kidney disease is not prohibitive for most proce-
dures. Mannitol may be used to minimize oliguric uremia in aortic operations.
Graft thrombosis is one of the leading local complications follow open revas-
cularizations. The etiology of graft thrombosis following bypass varies based
on its timing following surgery. Early graft thrombosis is most often due to a
technical issue, and should be addressed immediately with thrombectomy of
the graft and revision of any technical problems. If no technical issues are dis-
covered, patients are most often anticoagulated, and a hypercoagulable work‐
up is performed postoperatively. Graft thrombosis within the first 2 years but
out of the immediate postoperative period is most often due to neointimal
hyperplasia. To treat thrombosis after the immediate postoperative period,
grafts may be thrombectomized and an angiogram performed to determine
any areas of stenosis. Further open or endovascular treatment then depends on
the angiogram findings. Graft thrombosis after 2 years is most often due to
progression of the underlying disease.
Graft infection is a rarer but more dreaded complication. It occurs in 1–5%
of grafts [24, 41] and may require complete removal of the graft, especially if it
is a prosthetic conduit. Staphylococcus epidermidis and methicillin‐sensitive
Staphylococcus aureus are the most common pathogens isolated [41], although
other causative pathogens can include more virulent organisms, such as methi-
cillin‐resistant Staphylococcus aureus (MRSA). In the case of an infected pros-
thetic bypass, an extra‐anatomic bypass may be required in addition to removal
of the prior bypass in order to stay out of the infected field. This is ideally
performed with vein, although alternatives include rifampin‐soaked prosthetic,
antibiotic beads, or cadaveric homograft if vein is not available.
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Conclusion 175
Anastomotic aneurysms can occur at either the proximal or distal anastomo-
sis of a bypass graft. These are due to native arterial degeneration, infection, or
mechanical stress. If these are small, they may be observed. If they are large,
repair is mandatory due to the risk of rupture. The most pressing concern in
the case of an anastomotic aneurysm is whether it occurred due to infection,
particularly if there is any prosthetic within the operative field.
Aortic surgery carries its own unique set of complications. An aorto‐enteric
fistula is a rare entity, occurring in < 2% of all aortic operations [42], but it is a
dramatic complication with a high rate of mortality. It most often occurs at the
distal duodenum. Patients may have a herald bleed followed by exsanguination.
The treatment is graft removal and extra‐anatomic bypass or an in situ bypass
with rifampin‐soaked prosthetic or a cadaveric homograft. The affected intes-
tine must also be removed. A less dramatic but also distressing complication of
aortic surgery is erectile dysfunction due to lack of blood flow to the internal
iliac arteries. Disruption of per‐aortic nerve fibers can also produce retrograde
ejaculation.
Preoperative Evaluation and Management
The biggest concern in patients with PAD is their risk of cardiac complications.
According to joint guidelines from the AHA/ACC [43], the combination of the
surgical procedure and the individual patient’s clinical risk factors dictate what,
if any, formal cardiac testing they should undergo prior to their planned inter-
vention. In general, for higher‐risk procedures, pharmacologic cardiac stress
testing may be recommended if a patient’s functional capacity is difficult to
determine. This is often the case in vascular patients whose ability to ambulate
is limited by the very disease for which they seek treatment.
The fundamentals of medical therapy should not be overlooked as part of the
per‐operative preparation for an open or endovascular procedure. Smoking
cessation improves outcomes and reduces the risk of long‐term complications.
Blood glucose control is important in patients with concomitant diabetes.
Management of hypertension and hyperlipidemia is also important in this
population with their high burden of comorbidities.
Conclusion
Patients with peripheral vascular disease tend to have a high burden of comor-
bidities and depending on the exact nature of their PAD, may benefit the most
from an open or endovascular procedure, or simply medical management.
Referral to a specialist for symptomatic patients can help to determine the best
course of action and confirm the diagnosis.
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8 Surgical Management ofPeripheral Artery Disease
176
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179
Peripheral Artery Disease, Second Edition. Edited by Emile R. Mohler and Michael R. Jaff.
© 2017 John Wiley & Sons Ltd. Published 2017 by John Wiley & Sons Ltd.
a
abdominal aortic aneurysm
(AAA) 41, 48
rupture
41
abdominal bruits 48–49
abdominal examination 48–49
abdominal pain 41–42
abnormal vascular reactivity 1
ACCF/AHA guidelines on endovascular
treatment
131–132
acrocyanosis 45
acrogeria 46
acute limb ischemia (ALI) 2
amputation rate 13
definition 3
mortality rate
13
prevalence and incidence 13
referral for surgical
management 165
symptoms (six Ps) 3, 44
Adson’s maneuver 52
age‐related incidence and prevalence of
PAD 5–8
age, risk factor for PAD 13–14
alcohol intake, PAD risk and
19
Allen test and reverse Allen test 50
amaurosis fugax 38
amputation
in acute limb ischemia 13
in critical limb ischemia 12, 131
smoking risk factor in PAD
15
anemia
47
angiosomes 154–155
of the foot and lower leg 135–136,
138
angiotensin‐converting enzyme (ACE)
inhibitors
112, 113
angiotensin receptor blockers
(ARB)
112, 113
ankle–brachial index (ABI) 37
and segmental pressures 63–65
antiphospholipid antibodies, PAD risk
and
19
antiphospholipid syndrome 45
antiplatelet agents, studies
116–117
anxiety, risk factor for PAD
19
aortic aneurysm
46
chest examination 48
aortic dissection 40
aortic rupture
40
aortic surgery, risks related to 175
aortic valve regurgitation 40
aortobifemoral bypass
167–168
aorto‐iliac bypass 169
aorto‐iliac endarterectomy 169
aorto‐iliac interventions 145–147
angioplasty versus
stenting 146–147
PTFE‐covered versus bare metal
balloon‐expandable stents 147
Index
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Index
180
aorto‐iliac PAD 119
aorto‐iliac revascularization
167–169
arterial insufficiency
assessment 51–52
arterial tortuosity
46
arterial ulcers
49
arterial ultrasound imaging 1–2
arteria lusoria 40
arterial wall dysplasia
1
arteriosclerosis obliterans 1
ascending aorta dissection 40
aspirin 116–117, 141, 143
asymptomatic PAD 2
prevalence and incidence 8–10
atherectomy 152–153
atheromatous embolization
47
atherosclerosis 1
development of 1–2
eye examination 47
risk factor for PAD 13
risk factors 2
subclinical
1–2
atherosclerotic risk factor medical
management 111–117
antiplatelet agents 116–117
diabetes mellitus 113–114
hyperlipidemia 114
hypertension
112–113
smoking cessation 114–116
atypical leg pain
definition 2–3
prevalence and incidence 12
auscultation
for bruits 52–53
carotid artery 47
awareness of PAD in the
community 20–21
axillobifemoral bypass 168–169
b
bare metal balloon‐expandable
stents 147
Behçet’s disease 50
beta‐blockers
112
bivalirudin
140–141
blood pressure
46
medical management
112–113
blood pressure measurement, history
of
58–59
BMI, and PAD risk 14, 17–18
bowel infarction 41
bruit occlusion test
53
bruits
abdominal 48–49
auscultation for 52–53
detection of 47–48
Buerger’s disease 49–50, 115
Buerger’s test 51
bupropion
115
bypass operations, PAD risk and 19
c
cadmium, serum levels and PAD risk 19
calcium channel blockers
113
capillary refill test 51
cardiovascular accidents 38–39
cardiovascular disease, risk factor for
PAD 14
carotid arterial pulse 47
carotid artery bruits 47, 52
carotid intimal medial
thickness 1–2, 68
central cyanosis
46
cephalic index 46
cerebrovascular disease risk in
PAD 111–112
chest examination 48
chest veins, dilated 46
chilblains
45
cholesterol deposits in arteries 1–2
cholesterol levels
high cholesterol and PAD risk 14
risk factors for PAD 15–16
statin therapy 114
chronic exertional compartment
syndrome 96, 103
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Index 181
chronic kidney disease (CKD) 113
risk factor for PAD
19
cilostazol
118–120
classifications of PAD
42
claudication
42–44
classification systems
130
comparison of management
strategies
119–120
definition
2
hallmark symptom of PAD 2
pharmacotherapy 118
prevalence and incidence 10–11
when to refer for surgical
management 163–164
cleft palate 46
clinical syndromes of PAD
2–3
clopidogrel 116–117, 141, 143
color flow scans 68–69
community awareness of
PAD 20–21
computed tomography
angiography
73–77
advantages 76
anaphylaxis 77
artifacts 76
basics 73–74
calcification 76
contrast‐induced
nephropathy 76–77
image acquisition and
interpretation 74–75
pitfalls 76
protocol 74–75
radiation exposure
76
contrast‐induced nephropathy 82
conventional angiography 81–84
advantages
82
allergic reactions 81, 82
anaphylaxis 81, 82
artifacts 84
basics 81
digital subtraction angiography
(DSA) 82–83
image acquisition and
interpretation
81–83
informed consent
81
limitations
84
nephrogenic systemic fibrosis
82
pitfalls 82–84
pre‐procedure patient care 81
protocol 81–82
corneal arcus
46
coronary artery disease (CAD) risk in
PAD 111–112
costoclavicular maneuver 52
cough 40
covered stents in femoropopliteal
disease
151–152
C‐reactive protein (CRP), risk factor
for PAD
13, 14, 17
critical limb ischemia (CLI) 2, 44
ACCF/AHA guidelines on
endovascular
treatment
131–132
amputation risk
12, 131
classification systems 130
definition 3
endovascular treatment 131–132
indications for endovascular
therapy 131
limb prognosis
131
lower extremity wound
care 120–121
overall survival 131
patency issues 131
prevalence and incidence 12–13
typical anatomy in patients with
CLI 131
when to refer for surgical
management 164–166
cryoplasty 153
cutaneous vasculitis 50
cutis marmorata 45
cutting balloon angioplasty 153
cystic adventitial disease 96,
100–101
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Index
182
d
D‐dimer, association with PAD 17
deep vein thrombophlebitis
49–50
depression, risk factor for PAD
19
diabetes mellitus
eye examination 47
medical management 113–114
risk factor for atherosclerosis
2
risk factor for PAD 13, 14, 15
diagnostic approach, patients with leg
pain on exertion 104
Dieter test 39
differential diagnosis for PAD 92–94
digital subtraction angiography
(DSA)
82–83
digit ischemia 49–50
dolichocephaly 46
Doppler combined with 2D imaging
(duplex scanning)
68–69
Doppler ultrasound devices
functions
59
motion detection 59
waveform analysis 60
drug‐coated balloon (DCB) therapy in
femoropopliteal
disease
150–151
drug‐eluting stents in femoropopliteal
arteries 149–150
duplex scanning 67–69
background and history
67
color flow scans 68–69
Doppler (hemodynamic) 68–69
imaging (anatomy)
67–68
dyslipidemia, risk factor for
PAD
15–16
dysphagia
40, 41
aortica 40
lusoria 40
dyspnea 40–41
e
ectopia lentis 46, 47
Ehlers–Danlos syndrome 46
type IV
100
electronic cigarettes
115–116
embolus
44
enalapril
112
endovascular treatment of
PAD
129–156
access 138–139
anticoagulation 139–141
antiplatelet
management 141–143
aorto‐iliac interventions 145–147
background for endovascular
therapy
132–144
chronic total occlusions 143–144
clinical background 129–132
clinical evidence for peripheral
intervention 145–155
critical limb ischemia 131–132
femoropopliteal
interventions
147–153
history of development 129
indications for 129
intermittent
claudication 129–131
pedal interventions 153–155
peripheral arterial
anatomy
132–136
post‐procedural care 155
pre‐procedural imaging 136–138
radiation 143
re‐entry devices
143–144
technical background 136–144
tibioperoneal
interventions 153–155
vascular angiosomes of the foot and
lower leg 135–136, 138
end‐stage PAD 44
enophthalmos
46
epidemiology of PAD 1–26
erectile dysfunction, complication of
aortic surgery 175
ethnicity, PAD prevalence related
to 3–6
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